Cargando…

Bench-to-bedside review: Microvascular dysfunction in sepsis –hemodynamics, oxygen transport, and nitric oxide

The microcirculation is a complex and integrated system that supplies and distributes oxygen throughout the tissues. The red blood cell (RBC) facilitates convective oxygen transport via co-operative binding with hemoglobin. In the microcirculation oxygen diffuses from the RBC into neighboring tissue...

Descripción completa

Detalles Bibliográficos
Autores principales: Bateman, Ryon M, Sharpe, Michael D, Ellis, Christopher G
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2003
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC270719/
https://www.ncbi.nlm.nih.gov/pubmed/12974969
http://dx.doi.org/10.1186/cc2353
_version_ 1782121047484530688
author Bateman, Ryon M
Sharpe, Michael D
Ellis, Christopher G
author_facet Bateman, Ryon M
Sharpe, Michael D
Ellis, Christopher G
author_sort Bateman, Ryon M
collection PubMed
description The microcirculation is a complex and integrated system that supplies and distributes oxygen throughout the tissues. The red blood cell (RBC) facilitates convective oxygen transport via co-operative binding with hemoglobin. In the microcirculation oxygen diffuses from the RBC into neighboring tissues, where it is consumed by mitochondria. Evidence suggests that the RBC acts as deliverer of oxygen and 'sensor' of local oxygen gradients. Within vascular beds RBCs are distributed actively by arteriolar tone and passively by rheologic factors, including vessel geometry and RBC deformability. Microvascular oxygen transport is determined by microvascular geometry, hemodynamics, and RBC hemoglobin oxygen saturation. Sepsis causes abnormal microvascular oxygen transport as significant numbers of capillaries stop flowing and the microcirculation fails to compensate for decreased functional capillary density. The resulting maldistribution of RBC flow results in a mismatch of oxygen delivery with oxygen demand that affects both critical oxygen delivery and oxygen extraction ratio. Nitric oxide (NO) maintains microvascular homeostasis by regulating arteriolar tone, RBC deformability, leukocyte and platelet adhesion to endothelial cells, and blood volume. NO also regulates mitochondrial respiration. During sepsis, NO over-production mediates systemic hypotension and microvascular reactivity, and is seemingly protective of microvascular blood flow.
format Text
id pubmed-270719
institution National Center for Biotechnology Information
language English
publishDate 2003
publisher BioMed Central
record_format MEDLINE/PubMed
spelling pubmed-2707192003-11-21 Bench-to-bedside review: Microvascular dysfunction in sepsis –hemodynamics, oxygen transport, and nitric oxide Bateman, Ryon M Sharpe, Michael D Ellis, Christopher G Crit Care Review The microcirculation is a complex and integrated system that supplies and distributes oxygen throughout the tissues. The red blood cell (RBC) facilitates convective oxygen transport via co-operative binding with hemoglobin. In the microcirculation oxygen diffuses from the RBC into neighboring tissues, where it is consumed by mitochondria. Evidence suggests that the RBC acts as deliverer of oxygen and 'sensor' of local oxygen gradients. Within vascular beds RBCs are distributed actively by arteriolar tone and passively by rheologic factors, including vessel geometry and RBC deformability. Microvascular oxygen transport is determined by microvascular geometry, hemodynamics, and RBC hemoglobin oxygen saturation. Sepsis causes abnormal microvascular oxygen transport as significant numbers of capillaries stop flowing and the microcirculation fails to compensate for decreased functional capillary density. The resulting maldistribution of RBC flow results in a mismatch of oxygen delivery with oxygen demand that affects both critical oxygen delivery and oxygen extraction ratio. Nitric oxide (NO) maintains microvascular homeostasis by regulating arteriolar tone, RBC deformability, leukocyte and platelet adhesion to endothelial cells, and blood volume. NO also regulates mitochondrial respiration. During sepsis, NO over-production mediates systemic hypotension and microvascular reactivity, and is seemingly protective of microvascular blood flow. BioMed Central 2003 2003-07-28 /pmc/articles/PMC270719/ /pubmed/12974969 http://dx.doi.org/10.1186/cc2353 Text en Copyright © 2003 BioMed Central Ltd
spellingShingle Review
Bateman, Ryon M
Sharpe, Michael D
Ellis, Christopher G
Bench-to-bedside review: Microvascular dysfunction in sepsis –hemodynamics, oxygen transport, and nitric oxide
title Bench-to-bedside review: Microvascular dysfunction in sepsis –hemodynamics, oxygen transport, and nitric oxide
title_full Bench-to-bedside review: Microvascular dysfunction in sepsis –hemodynamics, oxygen transport, and nitric oxide
title_fullStr Bench-to-bedside review: Microvascular dysfunction in sepsis –hemodynamics, oxygen transport, and nitric oxide
title_full_unstemmed Bench-to-bedside review: Microvascular dysfunction in sepsis –hemodynamics, oxygen transport, and nitric oxide
title_short Bench-to-bedside review: Microvascular dysfunction in sepsis –hemodynamics, oxygen transport, and nitric oxide
title_sort bench-to-bedside review: microvascular dysfunction in sepsis –hemodynamics, oxygen transport, and nitric oxide
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC270719/
https://www.ncbi.nlm.nih.gov/pubmed/12974969
http://dx.doi.org/10.1186/cc2353
work_keys_str_mv AT batemanryonm benchtobedsidereviewmicrovasculardysfunctioninsepsishemodynamicsoxygentransportandnitricoxide
AT sharpemichaeld benchtobedsidereviewmicrovasculardysfunctioninsepsishemodynamicsoxygentransportandnitricoxide
AT ellischristopherg benchtobedsidereviewmicrovasculardysfunctioninsepsishemodynamicsoxygentransportandnitricoxide